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芦丁,一种胡芦巴糖苷,通过调节 NF-κB/IkBα 和 AMPK/ACC 通路改善了肥胖诱导的糖尿病肾病小鼠的病情。

Vitexin, a fenugreek glycoside, ameliorated obesity-induced diabetic nephropathy via modulation of NF-κB/IkBα and AMPK/ACC pathways in mice.

机构信息

Department of Endocrinology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China.

Department of Anesthesiology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China.

出版信息

Biosci Biotechnol Biochem. 2021 Apr 24;85(5):1183-1193. doi: 10.1093/bbb/zbab012.

DOI:10.1093/bbb/zbab012
PMID:33704405
Abstract

Obesity is one of the most critical risk factors for diabetes mellitus and plays a significant role in diabetic nephropathy (DN). The present investigation aimed to evaluate the possible mechanism of action of vitexin on obesity-induced DN in a high-fat diet (HFD)-fed experimental C57BL/6 mice model. Obesity was induced in male C57BL/6 mice by chronic administration of HFD, and mice were concomitantly treated with vitexin (15, 30, and 60 mg/kg, p.o.). HFD-induced increased renal oxido-nitrosative stress and proinflammatory cytokine levels were significantly inhibited by vitexin. The Western blot analysis suggested that alteration in renal NF-κB, IκBα, nephrin, AMPK, and ACC phosphorylation levels was effectively restored by vitexin treatment. Histological aberration induced in renal tissue after chronic administration of HFD was also reduced by vitexin. In conclusion, vitexin suppressed the progression of obesity-induced DN via modulation of NF-κB/IkBα and AMPK/ACC pathways in an experimental model of HFD-induced DN in C57BL/6J mice.

摘要

肥胖是糖尿病的最重要危险因素之一,在糖尿病肾病(DN)中起重要作用。本研究旨在评估牡荆素对高脂肪饮食(HFD)喂养的 C57BL/6 实验小鼠肥胖诱导型 DN 的可能作用机制。通过慢性给予 HFD 诱导雄性 C57BL/6 小鼠肥胖,同时用牡荆素(15、30 和 60 mg/kg,po)进行治疗。牡荆素显著抑制 HFD 诱导的肾脏氧化应激和促炎细胞因子水平升高。Western blot 分析表明,牡荆素治疗有效恢复了肾脏 NF-κB、IκBα、nephrin、AMPK 和 ACC 磷酸化水平的改变。牡荆素还减少了慢性给予 HFD 后肾组织的组织学异常。总之,牡荆素通过调节 NF-κB/IkBα 和 AMPK/ACC 通路抑制肥胖诱导的 DN 的进展,在 C57BL/6J 小鼠的 HFD 诱导的 DN 实验模型中。

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